We have demonstrated reversible inhibition of spermatogenesis and steroidogenes in normal men taking a potent gonadotropin-releasing hormone agonist, D-Trp6-Pro9-N-Ethylamide LHRH (LRFA). This proposal is designed to dissect the mechanism by which LRFA exerts its effects on te pituitary-gonadal axis in normal men, and to determine whether deleterious alterations in lipid metabolism occur as a result of LRFA-initiated hypogonadism in normal men. The specific questions which this proposal will address in normal male subjects treated with LRFA for 20 weeks are: (1) Is there a reduction in pituitary gonadotgrpin secretion? (2) Is there a reduction in the bioactivity of circulating LH? (3) Is the responsiveness of the pituitary gonadotroph to native LHRH compromised? (4) What is the pattern of steroid secretion? (5) Is gonadal responsiveness to exogenous hLH retained? (6) Is there an influence of frequency and dosage of LRFA treatment on responsiveness of the pituitary-gonadal axis? (7) What are the effects of serum lipids of LRFA-initiated hypogonadism in normal males? All studies will be carried out in normal males who will defer planned vasectomy for the duration of the studies. Blood samples will be collected for selected analysis of gonadotropins, steroids and precursors, and serum cholesterol, triglyceride and apoprotein concentrations.